卵巢癌手术切除难以清除微小病灶，而化疗的肿瘤细胞耐药性及全身毒副作用限制肿瘤治疗，导致肿瘤复发和转移。寻找合适的肿瘤位点靶向递送化疗药物同时调控肿瘤微环境是很好的策略。我们首次选用与选择性高表达于卵巢癌细胞的CXCR4受体具有高度亲和力的拮抗剂AMD3100为靶向头基，构建AMD-PEG-BSA-Gd新型纳米递药系统，以期在靶向递送紫杉醇至肿瘤部位的同时阻断CXCL12/CXCR4轴，逆转其招募免疫抑制细胞，促进肿瘤细胞生长转移的作用，增大化疗药物敏感性。前期工作已证实该递药系统可选择性靶向于表达CXCR4受体的卵巢癌细胞，而不靶向正常卵巢细胞，并初步明确其体外抗肿瘤活性，进一步研究将通过流式分析、51Cr释放实验、基因芯片等技术探讨该递药系统选择性减少肿瘤部位免疫抑制细胞Treg、MDSC，促进杀伤性免疫细胞的活性，及其抗卵巢癌生长转移的具体作用和机制，为减少卵巢癌复发转移提供新的思路。

Recurrence and metastasis of ovarian cancer were the leading cause of death. On the one hand, surgical resection was difficult to remove small lesions, on the other hand, tumor cell resistance and systemic side effects produced during conventional chemotherapy limited tumor therapy. It was a good strategy to find a suitable site on tumor cells for targeted delivery of chemotherapy drugs while regulating the tumor microenvironment. So we first selected AMD3100, an antagonist with high affinity to CXCR4 receptor which highly expressed on ovarian cancer cells as the targeting head group, then built a new type of AMD-PEG-BSA-Gd nano-drug delivery system, in order to deliver paclitaxel to tumor cells, at the same time, inhibit tumor growth and metastasis, reverse recruitment of immunosuppressive cells and increase sensitivity to chemotherapy drug through blocking the CXCL12/CXCR4 axis. Our previous work had confirmed that the delivery system could selectively target ovarian cancer cells which expressed CXCR4 receptor, while couldn't target normal ovarian cells, and initially revealed its anti-ovarian cancer activity in vitro. In the next study, we will use flow analysis, 51Cr Release assay, gene chip and other techniques to in-depth uncover the anti-tumor effect and mechanism of the drug delivery system, including selectively reducing the immunosuppressive cells Treg, MDSC at the tumor site to promote the activity of killer immune cells, inhibiting tumor growth and metastasis. In all, our research in this project will provide a new idea of treatment to reduce the recurrence and metastasis of ovarian cancer.